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ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

ABSTRACT: ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

PROVIDER: PRJEB32078 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3266322.fastq.gz	Fastqsanger.gz
	ERR3266323.fastq.gz	Fastqsanger.gz
	ERR3266324.fastq.gz	Fastqsanger.gz
	ERR3266325.fastq.gz	Fastqsanger.gz
	ERR3266326.fastq.gz	Fastqsanger.gz

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ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

Project description:ChIPseq of enterocytes of the jejunum from transgene C57BL/6 mice to assess the effects of a CKIαΔgut knock-out in the jejunum and a CKIαΔgut/p53 double knock-out. In addition, enterocytes expressing a mutant p53 (R172H) in combination with CKIαΔgut knockout were analyzed.

2020-02-25 | E-MTAB-7858 | biostudies-arrayexpress

RNAseq of enterocytes of the jejunum and Ileum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

Project description:RNAseq of enterocytes of the jejunum and Ileum from transgene C57BL/6 mice to assess the effects of a CKIα knock-out in combination with expression of a p53 mutant protein (R172H ) compared to a double knock-out of CKIα and p53. In addition, a group of mice exhibiting a CKIα knock-out and mutant p53 (R172H) was treated with gallic acid and compared to untreated mice (Jejunum only).

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RNAseq of enterocytes of the jejunum and Ileum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

Project description:RNAseq of enterocytes of the jejunum and Ileum from transgene C57BL/6 mice harboring a CKIαΔgut knock-out

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Transcription profiling of mouse intestinal epithelial spheroids cultured as stem cells, wound-associated epithelial cells or enterocytes

Project description:Intestinal epithelial spheroids were isolated from mouse jejunum as described in our previous publication (Miyoshi and Stappenbeck. In vitro expansion and genetic modification of gastrointestinal stem cells in spheroid culture. Nature Protocols. 2013. PMID: 24232249) and then grown in 50% L-WRN conditioned medium (for stem cells) or differentiation medium containing dmPGE2 (for wound-associated epithelial cells) or differentiation medium containing EP4 inhibitor (for enterocytes). Transcription profiling was performed to gain insight into the characteristics distinguishing these cell types.

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Effect of depletion of Drosophila Hepatocyte Nuclear Factor 4 (dHNF4) in enterocytes on gene expression in the adult midgut

Project description:The main objective of the sudy was to characterize the functions of Drosophila Hepatocyte Nuclear Factor 4 (dHNF4) in midgut enterocytes. For this, we expressed a UAS-dHNF4 RNAi transgene under the control of mex-GAL4, which is active specifically in midgut enterocytes. We then collected adult male midguts, extracted total RNA and performed mRNA-seq. Our data demonstrate that dHNF4 acts as a master regulator of intestinal lipid metabolism in Drosophila.

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Project description:RNAseq of enterocytes of the jejunum and Ileum from transgene C57BL/6 mice harboring a CKIÎ±Î”gut knock-out

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Chromosome-wide DNA unmethylome profiling examining human chromosomes 2, 9, 19 and mouse chromosomes 1, 9, 19

Project description:The unmodified DNA fraction of jejunal enterocytes and the jejunum lacking enterocytes of humans and jejunal enterocytes of mice was interrogated on Affymetrix tiling arrays

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Project description:Bisulfite padlock probe technique was used to examine DNA modifications at the lactase gene region for human and mouse tissues DNA modifications were investigated in human sperm, blood, jejunal enterocytes and jejunum lacking enterocytes, as well as mouse jejunal enterocytes and jejunum lacking enterocytes. For WGA samples, a genome devoid of DNA modifications was used to verify the efficiency of the bisulfite conversion reactions (the tissue sources were human or mouse intestine).

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Project description:Digested dietary fats are taken up, processed and transported by enterocytes to supply the body with lipids. Most absorbed lipids are assembled into pre-chylomicrons in the endoplasmic reticulum (ER) of enterocytes, which are then transported to the Golgi for maturation and subsequent secretion to the circulation. The role of mitochondria in regulating intestinal lipid transport remains unknown. Here we show that mitochondrial dysfunction in enterocytes inhibits chylomicron production and the transport of dietary lipids to peripheral organs. Mice with intestinal epithelial cell (IEC)-specific ablation of the mitochondrial-specific aspartyl - tRNA synthetase DARS2, as well as of the respiratory chain subunit SDHA or the assembly factor COX10 failed to thrive and showed massive accumulation of lipids within large lipid droplets (LDs) in enterocytes of the proximal small intestine (SI). Feeding a fat-free diet inhibited the formation of LDs in DARS2-deficient enterocytes, showing that accumulating lipids derive mostly from digested fat. Furthermore, metabolic tracing studies revealed impaired transport of dietary lipids to peripheral organs in mice lacking DARS2 in IECs. Moreover, DARS2-deficient enterocytes showed a distinct lack of mature chylomicrons concomitant with a disorganisation of the Golgi apparatus, suggesting that impaired ER to Golgi trafficking underlies impaired chylomicron production and secretion. Taken together, these results revealed a vital role of mitochondria in regulating dietary lipid transport in enterocytes, which is relevant for understanding the intestinal and nutritional defects observed in patients with mitochondrial defects.

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chipseq

Project description:chipseq data

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